The transcriptional control of LcIDL1–LcHSL2 complex by LcARF5 integrates auxin and ethylene signaling for litchi fruitlet abscission

At the physiological level,the interplay between auxin and ethylene has long been recognized as crucial for the regulation of organ abscission in plants.However,the underlying molecular mechanisms remain unknown.Here,we identified transcription factors involved in indoleacetic acid(IAA)and ethylene(ET)signaling that directly regulate the expression of INFLORESCENCE DEFICIENT IN ABSCISSION(IDA)and its receptor HAESA(HAE),which are key components initiating abscission.Specifically,litchi IDAlike 1(LcIDL1)interacts with the receptor HAESA-like2(LcHSL2).Through in vitro and in vivo experiments,we determined that the auxin response factor LcARF5 directly binds and activates both LcIDL1 and LcHSL2.Furthermore,we found that the ETHYLENE INSENSITIVE 3-like transcription factor LcEIL3 directly binds and activates LcIDL1.The expression of IDA and HSL2 homologs was enhanced in Lc ARF5and Lc EIL3 transgenic Arabidopsis plants,but reduced in ein3 eil1 mutants.Consistently,the expressions of LcIDL1 and LcHSL2 were significantly decreased in Lc ARF5-and LcEIL3-silenced fruitlet abscission zones(FAZ),which correlated with a lower rate of fruitlet abscission.Depletion of auxin led to an increase in 1-aminocyclopropane-1-carboxylic acid(the precursor of ethylene)levels in the litchi FAZ,followed by abscission activation.Throughout this process,LcRF5 and LcEIL3 were induced in the FAZ.Collectively,our findings suggest that the molecular interactions between litchi AUXIN RESPONSE FACTOR 5(LcARF5)-LcIDL1/LcHSL2 and LcEIL3–LcIDL1 signaling modules play a role in regulating fruitlet abscission in litchi and provide a long-sought mechanistic explanation for how the interplay between auxin and ethylene is translated into the molecular events that initiate abscission.

Regulation of aerobic glycolysis to decelerate tumor proliferation by small molecule inhibitors targeting glucose transporters

Dear Editor,Different from normal differentiated cells,metabolic reprogramming was spotted in cancer cells,due to increased demand for energy and macromolecule synthesis during their rapid proliferation(Hanahan and Weinberg,2011;Pavlova and Thompson,2016).Most cancer cells prefer anaerobic glycolysis even with oxygen in the environment due to its higher speed to produce macromolecular materials required for biosynthesis(Vander Heiden et al.,2009;DeBerardinis and Chandel,2016).But to compensate for the lower efficiency of anaerobic glycolysis in producing ATP,these cancer cells demand much higher glucose supply(Warburg,1956;Vander Heiden et al.,2009).These metabolic characteristics point to the huge demand of cancer cells for carbohydrate substrates,which creates the possibility of treating tumors by exploiting this feature(Patra et al.,2013;DeBerardinis and Chandel,2016).